Air pollution has been associated with increased risk of death and hospital admissions all over the world. Many of those associations are from cardiovascular disease, however the mechanism by which airborne particles increases the risk of cardiovascular deaths is still being explored. We looked at the effects of medium term and long term (annual mean) of particulate air pollution (PM2.5), ozone (O3), carbon monoxide (CO), and nitrogen dioxide (NO2), and changes in blood markers of cardiovascular risk, including HDL cholesterol, triglycerides and C-reactive protein, in the PRINCE study, a large, national randomized trial of the use of statins to lower such risk factors. A total of 5778 participants were matched to exposure from monitors in their county of resident.
We controlled for subject, trend, season, age, gender, race, body mass index, education, smoking history, hormone replacement therapy, exercise, and whether receiving a statin or a placebo.
We found a medium term (mean of the two previous months) effect between C-reactive protein and PM2.5, CO, NO2, with an increase of 7.7% (95% CI: 0.96-14.96) for 10 mg/m3 of PM2.5, an increase of 3.8% (95% CI: 0.3-7.3) for 5 ppm of NO2, an increase of 2.1% (95% CI: 0.1-4.1) for 0.5 ppm of CO. When we examined interactions with statin use we found a higher increase in subjects on placebo.
We found a significant association between triglycerides and the mean of the three previous months of ozone with an increase of 0.95% (95% CI: 0.1-1.8) for 5 ppm of O3. For the same time period for PM2.5, we found that the association was almost entirely in the subjects not receiving statins. In those subjects we found for the mean of the three previous months an increase of 8.3% (95% CI: 1.2-15.8).
For HDL cholesterol we fund an association with a longer averaging period (annual mean) of pollution, with a –3% increase (95% CI:-5.7- -0.3) for 10 mg/m3 of PM2.5 and a –1% increase (95% CI:-1.7- -0.3) for 5 ppm of O3.
These results present new the evidence of possible mechanism for the association between air pollution and cardiac events, and the cancellation of the effect by statins points to mechanistic pathways effected by statins.